Search

Meiosis is a differentiated program of the cell cycle that is characterized by high levels of recombination followed by two nuclear divisions. In fission yeast, the genetic program during meiosis is regulated at multiple levels, including transcription, mRNA stabilization, and splicing. Mei4 is a forkhead transcription factor that controls the expression of mid-meiotic genes. Here, we describe that Fkh2, another forkhead transcription factor that is essential for mitotic cell-cycle progression, also plays a pivotal role in the control of meiosis. Fkh2 binding preexists in most Mei4-dependent genes, inhibiting their expression. During meiosis, Fkh2 is phosphorylated in a CDK/Cig2-dependent manner, decreasing its affinity for DNA, which creates a window of opportunity for Mei4 binding to its target genes. We propose that Fkh2 serves as a placeholder until the later appearance of Mei4 with a higher affinity for DNA that induces the expression of a subset of meiotic genes., (Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.)

In the fission yeast Schizosaccharomyces pombe, meiosis is inhibited by the protein kinase Pat1, which phosphorylates and inactivates Mei2, an RNA binding protein essential for the initiation of meiosis. When diploid cells are deprived of nutrients, they initiate a cascade of events leading to the inactivation of Pat1 and entry into meiosis. Strains carrying the temperature-sensitive pat1-114 allele are forced to enter into meiosis when shifted to the non-permissive temperature, independently of the ploidity of the cell. This system has been extensively used, since it is possible to achieve a highly synchronous meiosis, which is a must for any molecular or microscopic approach that aims to decipher the mechanisms governing meiosis. Here, we have designed a new system to obtain a similarly synchronous meiosis, but independently of temperature shifts. Thus, by introducing a mutation in the ATP pocket of Pat1, we have generated a protein kinase that, in the presence of small specific inhibitors, can be inactivated. This results in forced entry into meiosis without the need of a temperature shift, minimizing the introduction of heat shock or any other stress responses along the meiotic waves of transcription.